Hypertension is one of the most common health concerns in the U.S. The National Institutes of Health estimates that 50 million or more Americans have high blood pressure, and a dramatic rise is anticipated as the baby boomer generation moves into maturity. Also by their estimate, worldwide prevalence of hypertension may exceed 1 billion. The NIH estimates that over 7 million deaths each year are attributable to hypertension and its complications.
Hypertension is a condition where the pressure of the blood in the vascular system, specifically the arterial system, is excessive. The body manages the flow and pressure of blood via a number of mechanisms. These include varying the capacity (the internal dimensions) of the arterial tree, varying the output of the heart, and managing the volume of fluid in the circulation, primarily a function of the kidneys. All of these are managed by the body in “real time,” i.e., on an ongoing basis – while we work, while we play, while we sleep.
“High blood pressure” or hypertension exists when blood pressure is in excess of 120/80 (or the recently revised 115/75), the first number being systolic pressure and the second, diastolic pressure. For either systolic or diastolic pressure to be high, one or more of the mechanisms that maintain blood pressure in a healthful range fail to perform their regulatory function.
All three mechanisms, arterial capacity, heart output, and kidney throughput, are automatically managed by the autonomic nervous system. Therefore, we can say that hypertension is an instance where the autonomic nervous system is either performing its task of managing blood pressure correctly – based on correct assessment of physiological status, it is performing its job in error. If it is the former, then it is the physiological status that is at issue. If it is the latter, then it could be considered a form of dysautonomia.
There is strong evidence that blood pressure is highly related to the “state” of the autonomic nervous system, where the state of excitation or “sympathetic” emphasis correlates highly with higher blood pressure and the state of relaxation or “parasympathetic” emphasis correlates highly with lower blood pressure. This makes sense because arterial capacity, heart rate, and heart output are directly under autonomic control. “Heart rate variability” (HRV), or the degree to which the heart rate varies, also correlates highly with autonomic status: lower variability correlates highly with sustained sympathetic bias and higher variability correlates with increased parasympathetic (vagal) action.
Heart rate variability is also known to correlate with respiration, where slower, deeper, more rhythmic respiration correlates highly with increased HRV and faster, shallower, more arrhythmic respiration correlates highly with diminished HRV. This raises two questions, a) Does blood pressure correlate with heart rate variability? b) Does blood pressure correlate with the frequency, depth, and rhythmicity of respiration?
In this article, researchers Elliott and Edmonson present preliminary findings regarding the first question, does blood pressure correlate with heart rate variability?
Their hypothesis is this… Slow, deep, rhythmic breathing results in the phenomenon of the respiratory arterial pressure wave (or more completely the arterio-venous wave) which is known to rise and fall by 20mmHg. (Medical Physiology, Guyton & Hall, 2002). The respiratory wave is depicted in the first and second red graphs at the top of Figure 1.
This respiratory arterio-venous wave is believed to be the physiological impetus for “breathing induced heart rate variability,” the bottom blue graph. Changes in blood flow and pressure resulting principally from respiration are detected by baroreceptors, specialized neurons distributed throughout major arteries. The autonomic nervous system uses baroreceptor input to coordinate heart rate, heart output, and vascular capacity to facilitate the respiratory wave. It is noted that other factors, e.g. stretch receptors in the chest, heart, etc. are also involved in this autonomic sensing and regulation.
When the arterio-venous wave is low, heart rate variability is low; when the arterio-venous wave is high, HRV is high. Neither the respiratory wave or its result, HRV, can be high if arteries are not relaxed during the exhalation phase of breathing. If arteries are relaxed during the exhalation phase of breathing, blood pressure cannot be high. Therefore, if correct, there should be an inverse correlation between HRV and blood pressure, i.e., high blood pressure and high HRV should be mutually exclusive, this being our hypothesis for Part I of the study.
The study consists of 103 instances of data collected from 42 clients after each engaged in 8-12 minutes of Coherent Breathing with HRV biofeedback. Because the Part I goal is simply to understand the real time relationship between blood pressure and HRV, both of which are considered variables, each assessment can be considered unique. It should be noted that 15/23 or 65% of hypertensives no longer demonstrated hypertensive pressures after the 8-12 minute period where the boundary is 100mmHg average blood pressure [(systolic+diastolic)/2]. As the impact of breathing with HRV biofeedback is a Part II consideration, those results will be presented in a future article.
Figure 2 presents the data, where it is seen that all of the data instances fall into the upper left, lower left, or lower right quadrants. There is one instance in the upper right but it is extremely close to the normo-tensive boundary of 100 mmHg. From this we can conclude that there are virtually no instances where average blood pressure is above normotensive and heart rate variability is above 13 beats. (HRV is measured in beats difference between the peak heart rate and the valley heart rate . The bottom graph of Figure 1 is an example of the heart rate varying.) The data is summarized by Figure 3.
The power trend line of Figure 2 curves gently upward as we move to the left, demonstrating stronger effect and nonlinearity in the relationship. In fact, if segmented there is a very dramatic difference in the correlation between blood pressure and HRV to the left and right of 13 beats, the correlation coefficient ≤13 beats being -0.62 and the correlation coefficient >13 beats being -0.05.
The linear trendline of Figure 4 demonstrates the strength of the effect ≤13 where we see that 1mmHg in average blood pressure relates to .3 beats of HRV; conversely, 1 beat of HRV relates to 3.3 mmHg average blood pressure. Again, please zoom in to see the graphic more clearly.
The large difference in correlation below vs. above 13 beats suggests that the physiological mechanisms of blood pressure and HRV are closely linked in lower HRV ranges and less so in higher HRV ranges. Additional research to confirm these results and further characterize this “range” is warranted. The data is reasonably supportive of the Part I hypothesis that high blood pressure and high HRV are mutually exclusive as there are no instances where blood pressure is above normo-tensive and HRV is above 20 beats (our “Hi” HRV boundary). The full report also presents systolic and diastolic pressures and their correlation with HRV. Please visit www.coherence.com for more details.
Stephen is life scientist and President, COHERENCE L.L.C. in Allen, Texas (www.coherence.com)
Dee Edmonson, R.N., BCIAC-EEG practices neurotherapy at the Neurotherapy Center of Plano. (www.neurologics.us)